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10.1152/ajpendo.00303.2014 http://scihub22266oqcxt.onion/10.1152/ajpendo.00303.2014 C4187027!4187027 !25117404     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25117404 &cmd=llinks): Failed to open stream: HTTP request failed! 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Vasodilator-stimulated phosphoprotein protects against vascular inflammation and insulin resistance |pdf=|usr=}}{{25117404 }} gab.com Text Vasodilator-stimulated phosphoprotein protects against vascular inflammation and insulin resistance JO: Am J Physiol Endocrinol Metab http://www.kidney.de/pget.php?&tw=1&pmid=25117404 #FOAvip Among the pleotropic effects of endothelial nitric oxide (NO) is protection against vascular inflammation during high-fat diet (HFD) feeding. The current work investigated the role of the enzyme vasodilatory-stimulated phosphoprotein (VASP) as a downstream mediator of the anti-inflammatory effect of NO signaling in vascular tissue. Relative to mice fed a low-fat diet (LFD), levels of VASP Ser(239) phosphorylation, a marker of VASP activation, were dramatically reduced in aortic tissue of mice with obesity induced by consuming a HFD. As reported previously, the effect of the HFD was associated with increased aortic inflammation, as measured by increased NF-?B-dependent gene expression, and reduced vascular insulin sensitivity (including insulin-stimulated phosphorylation of eNOS and Akt). These effects of the HFD were recapitulated by VASP knockout, implying a physiological role for VASP to constrain inflammatory signaling and thereby maintain vascular insulin sensitivity. Conversely, overexpression of VASP in endothelial cells blocked inflammation and insulin resistance induced by palmitate. The finding that transplantation of bone marrow from VASP-deficient donors into normal recipients does not recapitulate the vascular effects of whole body VASP deficiency suggests that the protective effects of this enzyme are not mediated in immune or other bone marrow-derived cells. These studies implicate VASP as a downstream mediator of the NO/cGMP pathway that is both necessary and sufficient to protect against vascular inflammation and insulin resistance. As such, this work identifies VASP as a potential therapeutic target in the treatment of obesity-related vascular dysfunction. Twit Text FOAVip Vasodilator-stimulated phosphoprotein protects against vascular inflammation and insulin resistance ????Am J Physiol Endocrinol Metab http://www.kidney.de/pget.php?&tw=1&pmid=25117404 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25117404 #FOAvip English Wikipedia <ref>{{Cite pmid|25117404 }}</ref> Vasodilator-stimulated phosphoprotein protects against vascular inflammation and insulin resistance #MMPMID25117404 Cheng AM ; Rizzo-DeLeon N ; Wilson CL ; Lee WJ ; Tateya S ; Clowes AW ; Schwartz MW ; Kim F Am J Physiol Endocrinol Metab 2014[Oct]; 307 (7 ): E571-9 PMID25117404 show ga Among the pleotropic effects of endothelial nitric oxide (NO) is protection against vascular inflammation during high-fat diet (HFD) feeding. The current work investigated the role of the enzyme vasodilatory-stimulated phosphoprotein (VASP) as a downstream mediator of the anti-inflammatory effect of NO signaling in vascular tissue. Relative to mice fed a low-fat diet (LFD), levels of VASP Ser(239) phosphorylation, a marker of VASP activation, were dramatically reduced in aortic tissue of mice with obesity induced by consuming a HFD. As reported previously, the effect of the HFD was associated with increased aortic inflammation, as measured by increased NF-?B-dependent gene expression, and reduced vascular insulin sensitivity (including insulin-stimulated phosphorylation of eNOS and Akt). These effects of the HFD were recapitulated by VASP knockout, implying a physiological role for VASP to constrain inflammatory signaling and thereby maintain vascular insulin sensitivity. Conversely, overexpression of VASP in endothelial cells blocked inflammation and insulin resistance induced by palmitate. The finding that transplantation of bone marrow from VASP-deficient donors into normal recipients does not recapitulate the vascular effects of whole body VASP deficiency suggests that the protective effects of this enzyme are not mediated in immune or other bone marrow-derived cells. These studies implicate VASP as a downstream mediator of the NO/cGMP pathway that is both necessary and sufficient to protect against vascular inflammation and insulin resistance. As such, this work identifies VASP as a potential therapeutic target in the treatment of obesity-related vascular dysfunction. |*Insulin Resistance/immunology [MESH] |Animals [MESH] |Aorta/cytology/immunology/*metabolism [MESH] |Bone Marrow Transplantation [MESH] |Cattle [MESH] |Cell Adhesion Molecules/genetics/metabolism/*physiology [MESH] |Cells, Cultured [MESH] |Diet, High-Fat [MESH] |Endothelial Cells/immunology/*metabolism [MESH] |Gene Expression Profiling [MESH] |Humans [MESH] |Inflammation/metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Microfilament Proteins/genetics/metabolism/*physiology [MESH] |Microvessels/cytology [MESH] |Nitric Oxide Synthase Type III/genetics [MESH] |Nitric Oxide/immunology/*metabolism [MESH] |Obesity/immunology/*metabolism [MESH] |Palmitates/pharmacology [MESH] |Phosphoproteins/genetics/metabolism/*physiology [MESH] |Phosphorylation [MESH] |Reverse Transcriptase Polymerase Chain Reaction [MESH] |Signal Transduction [MESH] |Vasculitis/immunology/*metabolism [MESH]Vasodilator-stimulated phosphoprotein protects against vascular inflam(epmc).pdf DeepDyve Pubget Overpricing